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22 Cards in this Set
- Front
- Back
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Gentamycin
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potential treatment for Muscular Dystrophy. MD results from a premature stop codon (dystrophin). Gentamycin allows for the skipping of this premature stop codon by binding when the stop codon is read during translation.
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What is the reason for the mechanistic cause of poliovirus?
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Polio virus has many of its messenger RNA that lack the 5' cap.
The virus, to compensate, uses a proteolysis molecule to kill the eIF4 protein in the host's (patient's) cells so that their non-capped RNA can compete better with ours….because eIF4 needs a 5' cap. |
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Eukaryotic initiation factor 4
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guides the mRNA to ribosome and it's Q is the 5' end. 7-methyl guanine cap is recognized by eIF4.
Extra Info: Just like the prokaryotes have a shine-delgarno sequence that initiates (by 16s) the translation process… Eukaryotes have a 5' cap on their mRNA -- this cap is recognized by an initation factor, eIF4, to start translation. |
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Characteristics of Diptheria toxin
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Point of slide:
• eukaryotics have an altered histidine amino acid called diphthamide (altered histidine side chain). • The diphtheria toxin targets this altered amino acid and changes it. • ADP ribosylation further alters it. • Resulting product is not able to be used as an elongation factor in protein synthesis, so it inhibits protein synthesis. • One would think we could delete the gene for this diphthamide a.a. -- but research shows that deleting this gene causes an increased risk of ovarian cancer. |
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Puromycin
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causes a premature STOP. This is the only mechanism he mentions.
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Streptomycin
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inhibits initiation
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Tetrocyclin
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binds to 30s subunit and inhibits 30s binding of aminoacyl-tRNA
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Erythromycin
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Binds to an inhibits 50s translocation
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Puromycin
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premature termination (acts as analog of aminoacyl-tRNA)
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Chloramphenicol
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inhibits peptidyl transferace (P site a.a. binding to A site A.A.) on 50s ribosomal subunit (prokaryot
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Cycloheximide
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inhibits peptidyl transferace (P site a.a. binding to A site A.A.) on 60s ribosomal subunit (prokaryot
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List the sites of the large ribosomal subunit:
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P site - peptideal (trna amino acid is positioned
A site - acceptor E site - exit. |
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Steps of protein synthesis:
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1. A.A preparation
2. Initiation 3. Elongation. 4. Termination 5. Post-translational processes. |
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What is shine-dalgarno sequence
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This is a sequence on a prokaryotic mRNA that is just upstream (5') of the start codon "AUG". There are many start codons in an mRNA, so the translation factors will prefer one that has the shine-dalgarno sequence before. This sequence is recognized by the 16s ribosome.
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What end of the tRNA are amino acids bound?
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the 3' end.
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What is aminoacyl-tRNA synthatase?
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aminoacyl-tRNA is a complex protein that ultimately brings the 2nd and on amino acids to the ribosome to create the polypeptide (the first amino acid methionine is brought by a met-tRNA complex). aminoacyl-tRNA synthatase simply uses ATP to bind the amino acid to the tRNA.
Modifying this could have potential therapeutically to bring alternate codons/aminoacids to the ribosome. |
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Stop codons are:
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U Go Away - UGA
U Are Away - UAA U Are Gone - UAG |
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Prokaryotic ribosome characteristics:
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Ribosome is characterized as 70s, made of a small (30s) and a large (50s) subunit.
• The large subunit is made of 31 proteins wrapped around a 23s rRNA and a 5s rRNA. • The small subunit is made of 21 proteins wrapped around a 16s rRNA. |
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miRNA
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it typically binds to the 3' end of the RNA and inhibits translation (but it can also promote translation).
• miRNA bind to the 3' end of the RNA and because the 3' end and 5' end are actually close together in the complex translation structure, the miRISC (or miRNA initiation suppressor complex) can actually inhibit transcription factors from binding at the 5' end. • miRNA bind to the 3' end of the RNA and can alter translation because it acts as a wall on the RNA that cannot be overcome by the ribosome as it continues down the strand during transcription. • important in cancer therapy. |
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HAT - histone actyltransferase - does what?
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starts translations by acetylating (adding acetyl groups or modifying the structure of) the histone tail and opening up the condensed chromosome.
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HDAC - histone deacetylase - does what?
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shuts down translations by deactylating the histone tail and causing the protein to stay condensed.
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The drug Gleevec is a treatment for "Philadelphia Chromosome". What does it do?
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Philadelphia Chromosome is a genetic disorder that results from the inappropriate recombination of chromosomes 22q and 9q. This disorder results in leukemia, but it is caused by ABL kinase being unregulated in patients with this condition. Gleevec will inhibit unregulated ABL Kinase.
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